Increased IL-33 expression in chronic obstructive pulmonary disease

Increased IL-33 expression in chronic obstructive pulmonary disease
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慢性阻塞性肺疾病中 IL-33 表达增加

DOI:
10.1152/ajplung.00305.2014
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发表时间:
2015-04-01
影响因子:
4.9
通讯作者:
Xie, Jungang
Xie, Jungang
中科院分区:
医学2区
文献类型:
--
作者:
Xia, Jie;Zhao, Junling;Xie, Jungang

文献摘要

被引文献

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慢性阻塞性肺疾病(COPD)是一种以炎性细胞活化和炎性介质释放为特征的炎性肺病。白细胞介素-33(IL-33)在各种炎症和免疫病理学中起关键作用,但缺乏其在COPD中作用的证据。本研究旨在探讨IL-33在COPD中的表达,并探讨IL-33是否参与COPD的发生和发展。ELISA法检测血清IL-33及其受体水平,COPD患者血清IL-33、ST 2和IL-1受体辅助蛋白水平均高于对照组。流式细胞术分析进一步证明了COPD患者中表达IL-33的外周血淋巴细胞(PBL)增加。免疫荧光分析显示,肺组织中IL-33的主要细胞来源是人支气管上皮细胞(HBE)。香烟烟雾提取物和脂多糖可增强PBLs和HBEs表达IL-33的能力。此外,来自COPD患者的PBL显示出响应于刺激的更大的IL-33释放。总的来说,这些发现表明,IL-33表达水平在COPD中增加,并且与气道和全身炎症相关。因此,IL-33可能有助于该疾病的发病机制和进展。
Chronic obstructive pulmonary disease (COPD) is an inflammatory lung disease characterized by inflammatory cell activation and the release of inflammatory mediators. Interleukin-33 (IL-33) plays a critical role in various inflammatory and immunological pathologies, but evidence for its role in COPD is lacking. This study aimed to investigate the expression of IL-33 in COPD and to determine whether IL-33 participates in the initiation and progression of COPD. Levels of serum IL-33 and its receptors were measured by ELISA, and serum levels of IL-33, ST2, and IL-1 receptor accessory protein were elevated in patients with COPD compared with control subjects. Flow cytometry analysis further demonstrated an increase in peripheral blood lymphocytes (PBLs) expressing IL-33 in patients with COPD. Immunofluorescence analysis revealed that the main cellular source of IL-33 in lung tissue was human bronchial epithelial cells (HBEs). Cigarette smoke extract and lipopolysaccharide could enhance the ability of PBLs and HBEs to express IL-33. Furthermore, PBLs from patients with COPD showed greater IL-33 release in response to the stimulus. Collectively, these findings suggest that IL-33 expression levels are increased in COPD and related to airway and systemic inflammation. Therefore, IL-33 might contribute to the pathogenesis and progression of this disease.